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Chronic intrauterine pulmonary hypertension increases capacitative calcium entry in fetal pulmonary artery smooth muscle cells

³Center of Excellence in Pulmonary Biology, Division of Pediatric Pulmonary, Allergy and Critical Care Medicine, Department of Pediatrics, Stanford University Medical School, Palo Alto, California; ¹Division of Pediatric Pulmonary and Critical Care Medicine, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota; and ²Department of Physiology, College of Medicine, Biomedical Engineering Program, Genomics Research Laboratory, University of Arizona, Tucson, Arizona

Submitted 24 August 2006 ; accepted in final form 1 December 2006

Oxygen causes perinatal pulmonary dilatation. Although fetal pulmonary artery smooth muscle cells (PA SMC) normally respond to an acute increase in oxygen (O₂) tension with a decrease in cytosolic calcium ([Ca²⁺]_i), an acute increase in O₂ tension has no net effect on [Ca²⁺]_i in PA SMC derived from lambs with chronic intrauterine pulmonary hypertension (PHTN). The present experimental series tests the hypothesis that an acute increase in O₂ tension decreases capacitative calcium entry (CCE) in normal, but not hypertensive, fetal PA SMC. PA SMC were isolated from late-gestation fetal lambs after either ligation of the ductus arteriosus (PHTN) or sham (control) operation at 127 days gestation. PA SMC were isolated from the distal PA (4th generation) and maintained under hypoxic conditions (25 Torr) in primary culture. After fura 2 loading, apparent [Ca²⁺]_i in PA SMC was determined as the ratio of 340- to 380-nm fluorescence intensity. Under both hypoxic and normoxic conditions, cyclopiazonic acid (CPA) increased [Ca²⁺]_i more in PHTN than in control PA SMC. CCE was determined in PA SMC under hypoxic and normoxic conditions, after superfusion with zero extracellular Ca²⁺ and intracellular store depletion with CPA, followed by superfusion with Ca²⁺-containing solution, in the presence of the voltage-operated calcium channel blockade. CCE was increased in PHTN compared with control PA SMC under conditions of both acute and sustained normoxia. Transient receptor potential channel gene expression was greater in control compared with PHTN PA SMC. PHTN may compromise perinatal pulmonary vasodilation, in part, by modulating PA SMC CCE.

cytosolic calcium; oxygen sensing; persistent pulmonary hypertension of the newborn

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